In the forests of northeastern Connecticut, Yale PhD student Steve Brady stood in black muck. He scooped up a handful of spotted salamander eggs. He had once imagined himself zipping across tropical waters or searching for exotic birds in rainforests. Instead, he started his career as an evolutionary biologist in a muddy ditch.

The eggs might have looked like any other salamander eggs from a woodland pond. But they weren’t, and this was no crystal-clear pool of water. It was a roadside puddle. If Brady was right, the toxic mixture associated with road runoff had forced the spotted salamanders to evolve over decades. In the time since Neil Armstrong first set foot on the Moon in 1969, these animals had been reinvented by nature to cope with their environment.

Adult salamanders look like creatures from an old horror movie. They are black with brilliant yellow spots, they have thick tails, and they walk slowly. And although the chemicals that might be responsible for their evolution are quite different from the atomic radiation used in those horror movies, Brady’s research suggests that this basic science-fiction idea—rapid evolution as a way of surviving exposure to toxic chemicals — is based on reality.

Roadside ponds are harsh places. “The chance of survival in a roadside pool is much lower than in a woodland pool,” Brady told me. “Even in adapted populations, [only] a little over half the eggs survived the first 10 weeks of development.” That’s a major hurdle, especially for wetland amphibians that already face intense natural challenges. Brady continued: “These pools frequently dry up before the animals have reached [maturity], leading to the loss of an entire generation.” And as the pools dry up, the contaminants in them — metals and salts, for the most part — become concentrated and increasingly toxic.

Steve Brady was curious about how populations could survive such harsh conditions. He designed a study, a sort of “switched at birth” for salamanders. Brady collected freshly laid eggs from both woodland and roadside ponds. He put some eggs from each environment into the woodland water and others into roadside pond water. He watched the creatures from the time they hatched through their early stages of development. The roadside salamanders out-lived woodland salamanders in a pattern that suggested the roadside populations had adapted to their harsh conditions.

We’re used to thinking of evolution as the very slow meandering transformation of life from single cells to complex beings, one random mutation at a time. This is evolution on a large scale. But large changes are often the visible expression of an accumulation of many small but significant ones. These changes can spread through one population and then another within our lifetime. This is evolution on a small scale. It is as old as life, but it is a phenomenon that we have been slow to understand.

When Alexander Fleming won the Nobel Prize in 1945 for discovering the antibiotic penicillin, he warned that using the drug too freely could lead to it becoming ineffective. Fifty years later, we are dealing with the result of overuse of penicillin and other antibiotics. Dangerous bacteria are becoming immune to our drugs.

Today, we know how and why bacteria become immune. In 1945, Fleming could not have known the biochemical details of how this might happen, but he did understand what it meant. Ongoing exposure to toxic chemicals is enough to drive the evolutionary process. The peppered moths of early industrial England are one example of this. As trees became blackened with soot from the new factories that had sprung up, the darker populations of the moths survived, while the lighter ones died, because they were easier to see. Later, the process reversed as new regulations decreased the amount of soot in the air. Instead of being seen as examples of rapid (or, more accurately, contemporary) adaptation, the peppered moths used to be thought of as an odd case of evolution brought about by human activity. We now know that those moths have plenty of company, including antibiotic-proof bacteria and pesticide-resistant insects.

Compared to many insects, vertebrates (animals with spines) have longer lives, with more time between generations. They also have smaller numbers of offspring. As a result, it has been harder to tell if they, like bacteria and insects, can experience this rapid evolution. Is it possible that the genetic makeup of vertebrates are not as resistant to change as we once thought? Perhaps, like the peppered moths, the salamanders are signs of discoveries to come. It might even be that rapid evolution in response to toxic chemicals is quite common.

Which raises questions like, what is the capacity for contemporary evolution? Can any species do it, or are some more likely than others to evolve? And if they are, what can we learn from them? Perhaps they are simply more prone to mutation. Perhaps their populations are more diverse, equipped with a larger pool of genes capable of weathering all sorts of environmental stresses.

This has been shown in other vertebrates, like some fish populations that have adapted to industrial-age chemicals such as PCBs and dioxins, which were rare before the last century.

So, what about us? You only need to skim the daily news to know that we all are breathing, bathing, eating, and drinking chemicals. Relatively rapid evolution does exist in humans. One of the best-known examples has to do with lactose intolerance—or actually, lactose tolerance. The ability of many humans to tolerate lactose is the result of a set of old genes that turned out to be beneficial for populations living a pastoral lifestyle. Even in that example, though, we aren’t talking about decades or a century for the adaptation to spread; it took many generations and perhaps thousands of years.

Some even question whether humans are still evolving. They wonder if we’ve stepped so far beyond the bounds of nature that we’ve interfered with our own evolutionary process. To some degree, human culture, medicine, and technology have indeed let us sidestep natural selection — a good thing for those of us who might not otherwise have survived. Even so, according to the evolutionary biologist Stephen Stearns and colleagues, we have not yet become an unchanging species. “Traits in many human populations,” they write, “are subject to natural selection, and have the genetic potential to respond to it…” At the very least, certain characteristics (height, for example) remain susceptible to selection, which means that we have not yet become a post-evolutionary species.

So we are evolving, though perhaps not so rapidly that it is detectable within a few generations. And even if we could evolve as rapidly as a salamander, the question remains: are we actually exposed to industrial toxins that are sufficiently persistent, powerful, or widespread to nudge our evolutionary process along? The consequences of not adapting to roadside salt are clear for salamanders — reduced fitness. What toxic selection pressures are acting upon us?

The good news is that we have limited our exposure to some industrial contaminants. PCBs were banned in the 1970s, and the production and release of other potentially harmful chemicals are, if not restricted, at least being investigated. Yet there are tens of thousands of industrial chemical contaminants, and we are continually releasing new products.

One complicating factor comes from new insights we’re now getting into the evolutionary process. It turns out that lifetime experiences such as environmental stress and diet can alter the way genes are expressed (for example, they may be turned on or off), and these changes can be passed down to subsequent generations without any alteration of the cells’ DNA sequence. This means that future generations might inherit a change that is heavily influenced by a single generation’s environmental conditions.

We also know that some toxic chemicals cause changes in gene expression, and that these changes can be inherited. The biologist David Crews and colleagues recently showed that exposing pregnant laboratory animals to the pesticide vinclozolin altered the weight, behavior, and stress responses of their offspring for up to three generations.

Genetically identical mice with different DNA methylation patterns causing changes in gene expression, in this case kinks in the tail of one but not the other. By Emma Whitelaw, University of Sydney, Australia, CC BY 2.5.

And so we now confront a possibility that is both intriguing and deeply troubling. Industrial chemicals might have negative effects that are widespread and inheritable, not only in humans but in all life on Earth.

When it comes to rapid evolution, we might not encounter pressures such as those that shaped Steve Brady’s roadside salamanders. But we certainly have not escaped the danger of chemical exposure. It is possible we could experience a kind of rapid response through chemically induced alterations to gene expression. How these will influence the evolution of humans is anybody’s guess. Perhaps they will be of little consequence. Perhaps the outcome will be so devastating that carriers of the altered gene expression are eventually weeded out. Or perhaps humans in the not-so-distant future will become actors in a real-life science fiction, fending off hordes of rapidly evolving chemical-resistant bacteria and insects, even as we are weakened through the accumulation of the many changes of our own making.